Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia

Abstract. Introduction:. Trigeminal neuralgia (TN) is a chronic, debilitating facial pain disease causing stabbing pain attacks in the sensory distribution of the trigeminal nerve. The underlying pathophysiology of TN is incompletely understood, although microstructural abnormalities consistent with...

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Main Authors: Curtis Ostertag, Timothy N. Friedman, Michael B. Keough, Bradley J. Kerr, Tejas Sankar
Format: Article
Language:English
Published: Wolters Kluwer 2023-12-01
Series:PAIN Reports
Online Access:http://journals.lww.com/painrpts/fulltext/10.1097/PR9.0000000000001117
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author Curtis Ostertag
Timothy N. Friedman
Michael B. Keough
Bradley J. Kerr
Tejas Sankar
author_facet Curtis Ostertag
Timothy N. Friedman
Michael B. Keough
Bradley J. Kerr
Tejas Sankar
author_sort Curtis Ostertag
collection DOAJ
description Abstract. Introduction:. Trigeminal neuralgia (TN) is a chronic, debilitating facial pain disease causing stabbing pain attacks in the sensory distribution of the trigeminal nerve. The underlying pathophysiology of TN is incompletely understood, although microstructural abnormalities consistent with focal demyelination of the trigeminal nerve root have been shown in patients with TN. Studies of the cerebrospinal fluid (CSF) in patients with TN suggest an increased prevalence of inflammatory mediators, potentially implicating neuroinflammation in the pathophysiology of TN, as it has been implicated in other chronic pain conditions. Objectives:. This study aimed to further assess the inflammatory profile of CSF in TN. Methods:. Cerebrospinal fluid was collected from 8 medically refractory patients with TN undergoing microvascular decompression surgery and 4 pain-free controls (2 with hemifacial spasm; 2 with normal pressure hydrocephalus). Cerebrospinal fluid was collected from the cerebellopontine angle cistern intraoperatively in the patients with TN. Inflammatory profiles of CSF samples were analyzed using a 71-plex cytokine and chemokine multiplex assay. Results:. Ten inflammatory markers were found to be significantly higher in TN CSF, and no analytes were significantly lower. Elevated factors can be classified into pro-inflammatory cytokines (IL-9, IL-18, and IL-33), chemokines (RANTES and ENA-78), the tumor necrosis factor superfamily (TRAIL and sCD40L), and growth factors (EGF, PDGF-AB/BB, and FGF-2). Conclusion:. This study further supports the notion that neuroinflammation is present in TN, and that multiple molecular pathways are implicated.
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spelling doaj.art-cf7a41355983480c800fb377afef527e2023-12-27T06:53:25ZengWolters KluwerPAIN Reports2471-25312023-12-0186e111710.1097/PR9.0000000000001117202312000-00021Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgiaCurtis Ostertag0Timothy N. Friedman1Michael B. Keough2Bradley J. Kerr3Tejas Sankar4a Cumming School of Medicine, University of Calgary, Calgary, AB, Canadab Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canadac Division of Neurosurgery, Department of Surgery, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canadab Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canadab Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, CanadaAbstract. Introduction:. Trigeminal neuralgia (TN) is a chronic, debilitating facial pain disease causing stabbing pain attacks in the sensory distribution of the trigeminal nerve. The underlying pathophysiology of TN is incompletely understood, although microstructural abnormalities consistent with focal demyelination of the trigeminal nerve root have been shown in patients with TN. Studies of the cerebrospinal fluid (CSF) in patients with TN suggest an increased prevalence of inflammatory mediators, potentially implicating neuroinflammation in the pathophysiology of TN, as it has been implicated in other chronic pain conditions. Objectives:. This study aimed to further assess the inflammatory profile of CSF in TN. Methods:. Cerebrospinal fluid was collected from 8 medically refractory patients with TN undergoing microvascular decompression surgery and 4 pain-free controls (2 with hemifacial spasm; 2 with normal pressure hydrocephalus). Cerebrospinal fluid was collected from the cerebellopontine angle cistern intraoperatively in the patients with TN. Inflammatory profiles of CSF samples were analyzed using a 71-plex cytokine and chemokine multiplex assay. Results:. Ten inflammatory markers were found to be significantly higher in TN CSF, and no analytes were significantly lower. Elevated factors can be classified into pro-inflammatory cytokines (IL-9, IL-18, and IL-33), chemokines (RANTES and ENA-78), the tumor necrosis factor superfamily (TRAIL and sCD40L), and growth factors (EGF, PDGF-AB/BB, and FGF-2). Conclusion:. This study further supports the notion that neuroinflammation is present in TN, and that multiple molecular pathways are implicated.http://journals.lww.com/painrpts/fulltext/10.1097/PR9.0000000000001117
spellingShingle Curtis Ostertag
Timothy N. Friedman
Michael B. Keough
Bradley J. Kerr
Tejas Sankar
Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
PAIN Reports
title Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
title_full Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
title_fullStr Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
title_full_unstemmed Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
title_short Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
title_sort heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia
url http://journals.lww.com/painrpts/fulltext/10.1097/PR9.0000000000001117
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